W10- Neuro: Somatosensation II Flashcards
What are the two major central pathways of the
somatosensory system
- Dorsal column-medial lemniscal system (DCML)
- Spinothalamic tract (anterolateral system) (STT)
What are the Ascending pathways mediating sensory aspects of pain for body and face
2nd order neurons decussate (cross or intersect each other to form an X) and project to ventral-posterior nuclear complex of
thalamus
* VPL: body
* VPM: face
Where does the DCML and STT cross?
DCML and STT cross the midline at different sites
Differential loss of temperature/pain vs fine tactile discrimination
There is a left and right part of the spinal cord.
If there was a lesion on the left side, it would cut through the white matter, so would interrupt the fibres of the anterolateral system and the DCML in the dorsal column. But not both will be effected the same. The DCML is from the mechanoreceptive afferents coming from the same left side of the body. The anterolateral column comes from Nociceptive afferents from the right side of the body (delta and c fibres). This means on the same side of the lesion, loss of tactile discrimination. On the opposite side, reduced sensation of temperature and pain.
What is pain?
Dual aspect model:
1. Sensory-discriminative
* Location
* Intensity
* Duration
* Quality
- Affective-motivational
* Unpleasantness – the painfulness of pain
* Effects on arousal, mood (affect), behaviour
What are the specialised receptors for pain detection?
Nociceptors are neurons specialized for detection of painful stimuli.
If we plot a graph with non-nociceptive thermoreceptors against temperature, it responds to temps around normal skin temperature, then it plateaus as the temp continues to increase.
Nociceptor thermoreceptors does not respond until the temp is closer to the threshold for painfully hot and continues to increase thereafter.
What do A-delta and C-fibres do?
A-delta and C-fibres contribute different aspects of pain sensation.
Eg. if you touch a hot metal radiator, there is an immediate first pain that makes us pull our hand away (A delta fiber) and a second wave of dull pain (C fiber).
What is TRPV1?
The TRPV1 receptor is involved in transduction of noxious heat
Originally called vanilloid receptor, present in A-δ and C-fibres.
This receptor is sensitive to other things aside from heat, which opens the sodium and calcium into the cell, resulting in depolarisation - ie. activation of the nociceptor.
Capsaicin also acts as an agonist to this receptor - the active ingredient in hot chilly.
What happens after an injury?
Maintenance of nociceptor activity after
injury ‘Inflammatory soup’ of cytokines, prostaglandins and small signalling molecules
maintains depolarisation and sensitivity of C-fibre terminals after original stimulus
* Hyperalgaesia = increased sensitivity to pain
* Allodynia = painful response to a normally innocuous stimulus. Eg, light touch to burned area.
These can either be released or are biproducts of tissue damage:
- ATP, Prostaglandin, Histamine, H+, 5-HT, Bradykinin, Substance P.
Substance synthesised and secreted by C fibres = Substance P.
What is the anterolateral system (STT)?
Dorsal horn interneurons
* Located in superficial and deep layers of dorsal horn
* Synaptic input from C- and A-δ fibres
* Axons cross and ascend in anterolateral white matter
* Some are multi-modal (receive convergent nociceptive and non-nociceptive inputs)
* Some receive convergent input from visceral afferents. Consequently, visceral signals are very poorly localised.
What referred pain?
Poorly localised pain.
Internal organ pains manifest in a way that is not obvious.
Eg. Heart pains like angina, felt in the neck, arm
The explanation of this is conversion of visceral afferents onto the second order interneurons receiving their c fibres or A delta fibres from that particular part of the body.
What is cortical representation of pain?
Cortical representation of pain is
complex
*STT projects to S1 via VP nuclei of thalamus (like DCML system)
*however, STT and DCML axons do not converge on same thalamic neurons – pathways are parallel
*S1 is necessary for the localization of pain, but stimulation of S1 gives rise to referred tactile, not painful, sensations
*Additional areas are involved in pain sensations
What are the two systems in central pain processing?
*Diverge at level of thalamus
*Lateral system (do not confuse with anterolateral system)
* VP nuclei of thalamus, in parallel with DCML system
* Primary and secondary somatosensory cortex (SI and SII)
*Medial system
* Midline nuclei of thalamus (intralaminar) projects onto the Anterior cingulate and insular cortex
What is the lateral and medial pain system? The anatomical basis for the two aspects of pain sensation?
Lateral
* Sensory-discriminative - anterolateral system to the ventral posterior nucleus to the somatosensory cortex.
* Project via specific somatosensory thalamic nuclei - required for discriminative side like location.
Medial
* Affective-motivational
* Project to different cortical areas via (non-specific) midline thalamic nuclei - projects to the anterior cingulate cortex and insular cortex. This is part of the limbic system (motivations/emotion etc). Maybe responsible for unpleasant side of pain.
What is pain?
Dual aspect model:
1. Sensory-discriminative
* Location
* Intensity
* Duration
* Quality
2. Affective-motivational
* Unpleasantness – the painfulness of pain
* Effects on arousal, mood (affect), behaviour
What are the descending modulation of pathways?
*Analgaesic properties of opium known for centuries
*Endogenous opioids (enkephalins, endorphins) and opioid receptors discovered 1970s-80s - initially assumed to exist since heroin, opium etc binds.
Opium are the derivatives of the most powerful pain killers known.
Main source of endogenous opioids = midbrain periaqueductal gray. These descend to structures associated with neuromodulation - especially serotonin and noradrenaline. Eg. serotonin will activate local spinal cord interneurons and contains opioids - presynaptically inhibit c fibres.
This is how an epidural anaesthetic work - injection of opioids directly into around the spinal cord.
